Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-18, previously designated interferon gamma-inducing factor, is a proinflammatory cytokine structurally related to interleukin-1beta and is therefore considered a member of the growing family of interleukin-1-like cytokines. Both interleukin-18 and -1beta are synthesized as inactive precursors that necessitate cleavage by caspase-1 for functional activity. In this study, the authors analyzed the expression pattern of interleukin-18, -1beta, and caspase-1 in focal brain ischemia induced in rats either by permanent middle cerebral artery occlusion or by photothrombosis of cortical microvessels. Using reverse transcriptase-polymerase chain reaction, they found a delayed increase of interleukin-18 mRNA starting at 48 hours and reaching its peak between 7 and 14 days after ischemia. In contrast, interleukin-1beta mRNA peaked within 16 hours and was downregulated thereafter. The time course of caspase-1 mRNA expression paralleled that of interleukin-18, but not of interleukin-1beta mRNA. Immunocytochemically, interleukin-18 expression was localized to ED1-positive phagocytic microglia/macrophages infiltrating the necrotic lesion between 3 and 6 days after ischemia. In contrast, interleukin-1beta immunoreactivity was expressed by ramified microglia in the infarct border zone and remote ipsilateral cortex during the first 16 hours postlesion. Induction of interleukin-18 was not accompanied by detectable expression of interferon-gamma mRNA. Their data show spatial and temporal diversity in interleukin-1 and -18 cytokine family expression in brain ischemia, and suggest a role of the interleukin-18/caspase-1 pathway in late-stage inflammatory responses to focal brain ischemia.
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PMID:Interleukin-18 expression after focal ischemia of the rat brain: association with the late-stage inflammatory response. 1180 95

The antiviral activity of recombinant bovine interferon gamma (rbIFN-gamma) against bovine leukaemia virus (BLV) was evaluated by an in vitro assay. rbIFN-gamma was prepared using a baculovirus expression system and replication of BLV was measured by syncytium assay. Antiviral effects were observed when bovine and sheep cells were used as target cells or effector cells and treated with 0.1 unit/ml of rbIFN-gamma. Formed syncytium numbers were reduced less than 1/20 when these cells were treated with 10 units/ml of rbIFN-gamma. However, the antiviral effects on cells of heterologous species were decreased and more than 1000 units/ml of rbIFN-gamma were required to induce an anti-BLV effect on the combination of CC81 cells as target cells and Bat2Cl6 cells as effector cells, which originated from the cat and bat, respectively. When the degree of BLV production was estimated by reverse transcriptase (RT) activity, no antiviral effect of rbIFN-gamma was induced soon after the treatment, but it was evident in the cells persistently infected with BLV. These results showed that rbIFN-gamma suppresses the replication of BLV in vitro, but has effective biological activity on cells of homologous species.
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PMID:Anti-viral effect of recombinant bovine interferon gamma on bovine leukaemia virus. 1188 26

Chemokines are important mediators of cell trafficking during immune inductive and effector activities, and dysregulation of their expression might contribute to the pathogenesis of human immunodeficiency virus type 1 and the related simian immunodeficiency virus (SIV). To understand better the effects of SIV infection on lymphoid tissues in rhesus macaques, we examined chemokine messenger RNA (mRNA) expression patterns by using DNA filter array hybridization. Of the 34 chemokines examined, the interferon gamma (IFN-gamma)-inducible chemokine CXC chemokine ligand 9/monokine induced by interferon-gamma (CXCL9/Mig) was one of the most highly up-regulated chemokines in rhesus macaque spleen tissue early after infection with pathogenic SIV. The relative levels of expression of CXCL9/Mig mRNA in spleen and lymph nodes were significantly increased after infection with SIV in both quantitative image capture and analysis and real-time reverse transcriptase-polymerase chain reaction assays. In addition, in situ hybridization for CXCL9/Mig mRNA revealed that the patterns of expression were altered after SIV infection. Associated with the increased expression of CXCL9/Mig were increased numbers of IFN-gamma mRNA-positive cells in tissues and reduced percentages of CXC chemokine receptor (CXCR) 3(+)/CD3(+) and CXCR3(+)/CD8(+) lymphocytes in peripheral blood. We propose that SIV replication in vivo initiates IFN-gamma-driven positive-feedback loops in lymphoid tissues that disrupt the trafficking of effector T lymphocytes and lead to chronic local inflammation, thereby contributing to immunopathogenesis.
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PMID:Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-gamma in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome. 1196 73

Atopic dermatitis is a common inflammatory skin disease of humans and dogs. Human atopic dermatitis is associated with T-helper (Th) 2 type responses, although Th1 cytokines are present in chronic lesions. This study used semi-quantitative reverse transcriptase polymerase chain reactions to determine the expression of gene transcripts for immunosuppressive cytokines (transforming growth factor beta [TGFbeta] and interleukin [IL]-10), Th2 type cytokines (IL-4 and IL-6) and Th1 type cytokines (interferon gamma [IFNgamma], tumour necrosis factor alpha [TNFalpha], IL-2 and IL-12) in lesional atopic, non-lesional atopic and healthy canine skin. Canine atopic dermatitis was associated with over-expression of IL-4 mRNA and reduced transcription of TGFbeta compared to healthy skin (ANOVA, p<0.05). Higher levels of IFNgamma, TNFalpha and IL-2 mRNA were seen in lesional compared to non-lesional and healthy skin (p<0.05). There were no significant differences in IL-10, IL-6 or IL-12 transcription. This is the first report to demonstrate that canine atopic dermatitis is associated with over-production of IL-4 and under expression of TGFbeta.
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PMID:T-helper 1, T-helper 2 and immunosuppressive cytokines in canine atopic dermatitis. 1207 61

Cytokines and beta-chemokines are important mediators of the immune system and are expressed in many infectious diseases. To study cytokine and beta-chemokine profiles during pathogenesis of lentiviral infection and progression to AIDS in rhesus macaques, we established new quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) assays based on TaqMan chemistry. Using synthetic RNA standards, we quantified mRNAs of IL-2, IL-4, IL-6, IL-10, IL-12 p40, interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), RANTES, macrophage inflammatory protein 1 alpha (MIP-1 alpha), and MIP-1 beta in unstimulated peripheral blood mononuclear cells (PBMCs) and lymph nodes from macaques chronically infected with SIV or SHIV. Viremic monkeys with decreased CD4(+) T cell counts (<500 cells/microl) had significantly higher IL-10 mRNA expression than uninfected controls, which parallels the findings in HIV-1-infected humans. In addition, MIP-1 alpha, MIP-1 beta, and RANTES mRNA expression increased in viremic monkeys with decreased CD4(+) T cell counts; gene expression was inversely correlated with CD4(+) T cell counts, but not viral load. The newly established quantitative real-time RT-PCR assays will allow the determination of cytokine and beta-chemokine patterns in rhesus macaques in studies of microbial pathogenesis or vaccine development.
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PMID:Quantitation of simian cytokine and beta-chemokine mRNAs, using real-time reverse transcriptase-polymerase chain reaction: variations in expression during chronic primate lentivirus infection. 1207 58

We previously demonstrated that cyclic ADP-ribose (cADPR) elicits Ca2+ release in airway smooth muscle (ASM) cells through ryanodine receptor channels. CD38 is a cell surface protein that catalyzes the synthesis and degradation of cADPR. In inflammatory diseases such as asthma, augmented Ca2+ responses and Ca2+ sensitivity contribute to increased ASM contractility in response to agonists. In this study, we investigated the regulation of CD38 expression and the role of cADPR-mediated Ca2+ release in airway inflammation. Human ASM cells in culture between the second and fifth passages were exposed to tumor necrosis factor alpha (TNF-alpha), interleukin 1beta, or interferon gamma, or bovine serum albumin (controls). CD38 expression was measured by reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, and Western blot analysis, and ADP-ribosyl cyclase activity was assayed with nicotinamide guanine dinucleotide as the substrate. Ca2+ responses to acetylcholine, bradykinin, and thrombin were measured in fura-2AM-loaded cells by fluorescence microscopy. Cytokines caused significant augmentation of CD38 expression, ADP-ribosyl cyclase activity, and Ca2+ responses to the agonists, compared with the control. TNF-alpha effects were greater than those of the other two cytokines. The cADPR antagonist 8-bromo-cADPR attenuated the Ca2+ responses to the agonists in control and cytokine-treated cells, with the magnitude of inhibition correlating with the level of CD38. This study provides the first demonstration of a role for CD38-cADPR signaling in a model of inflammatory airway disease.
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PMID:CD38/cyclic ADP-ribose-mediated Ca2+ signaling contributes to airway smooth muscle hyper-responsiveness. 1251 17

In this study, it is reported that neonatal murine microglia and N9 murine microglial cell line express tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). TRAIL protein and mRNA expression in murine microglia greatly upregulate upon stimulation with interferon gamma (IFNgamma) or lipopolysaccharide (LPS) as revealed by immunoprecipitation-immunoblotting, reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry techniques. IFNgamma and LPS act synergistically to induce TRAIL expression on both translational and transcriptional levels. The upregulated microglial TRAIL in inflammatory conditions may involve in the cytotoxic effect of these cells and play a role in neurodegenerative processes.
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PMID:Interferon gamma and lipopolysaccharide upregulate TNF-related apoptosis-inducing ligand expression in murine microglia. 1266 42

The development of effective, safe vaccines for human and bovine respiratory syncytial virus (RSV) has been problematic. Inactivated RSV vaccines are of variable efficacy; poor efficacy may be related to induction of ineffective cell-mediated immunity (CMI). To characterize CMI in calves vaccinated with formalin inactivated (FI) BRSV, 11 calves were vaccinated twice with FI-BRSV (n=5) or mock vaccine (n=6) at a 2 week interval and challenged 1 month later. Prior to challenge a cannula was placed in the efferent lymphatic of the caudal mediastinal lymph node of each calf; lymph derived lymphocytes (LDL) were collected for analysis of CMI. Cytotoxic T lymphocyte (CTL) activity by LDL and/or peripheral blood mononuclear cells (PBMC) was measured by 51Cr release on days 5, 7, 9, and 10 post-challenge. Messenger RNA for interferon gamma (IFN-gamma), interleukin 2 (IL-2) and IL-4 was measured on days 0-10 by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) of RNA of LDL. BRSV-specific IFN-gamma production by PBMC was measured on days 0 and 10 by ELISA. Clinical signs and postmortem changes following challenge were evaluated. There was no difference between groups in clinical signs, postmortem changes, CTL activity, cytokine message expression, or IFN-gamma production. For both groups, percentage lysis by CTL peaked on days 7-10 and ranged from 11 to 25%. Failure of vaccination to prevent disease following challenge was likely associated with failure to prime for improved CMI responses.
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PMID:Cytotoxic T lymphocyte activity and cytokine expression in calves vaccinated with formalin-inactivated bovine respiratory syncytial virus prior to challenge. 1465 42

Allograft function may become impaired during rejection after human liver transplantation. Cytokines induce nitric oxide (NO) production in hepatocytes, Kupffer cells and infiltrating mononuclear cells. NO inhibits cytoplasmatic cytochrome p450 (CYP) enzyme activity in vitro. It is not known whether this mechanism plays a role in vivo. In order to characterize the role of locally produced cytokines in the pathogenesis of liver dysfunction, we analysed human liver transplant biopsy material for the expression of proinflammatory cytokines as well as for NO synthase and we compared these results to the microsomal liver function in vivo [aminopyrine breath test (ABT)] and in vitro (enzymatic analysis of CYP). Microsomal liver function decreased in vivo during rejection while ABT levels decreased by 40% and increased again by 59% after the acute rejection episode. Similarly, CYP 1A2 and 2E1 activity dropped 42% and 24% in rejecting samples, respectively. Competitive reverse transcriptase polymerase chain reaction (RT-PCR) showed a fivefold upregulation of interferon gamma (IFN-gamma) gene expression. Inducible, but not constitutive NO-synthase gene expression was upregulated fivefold in samples from rejecting patients suggesting a local induction of NO in response to immune events. Our data show a marked impairment of CYP enzyme activity during allograft rejection which is presumably secondary to an increased intragraft production of proinflammatory cytokines and NO.
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PMID:Intragraft iNOS induction during human liver allograft rejection depresses cytochrome p450 activity. 1534 22

Porcine reproductive and respiratory syndrome virus (PRRSV) causes a prolonged active infection followed by a persistent infection in lymphoid tissues lasting for several months. Pigs develop both an antibody and cell-mediated immune response following PRRSV infection, but the specific role of each type in the development of protective immunity and clearance of the virus is not yet known. The aims of this study were to characterize the dynamics of PRRSV persistence from 0 to 135 d post infection (pi), characterize the kinetics of the antibody mediated immune response following PRRSV infection, and characterize the cell mediated immune responses to PRRSV infection. Eighty, 4-month-old PRRSV-free gilts were obtained from a source known to be negative for PRRSV. On day 0, gilts were infected intranasally with 10(2.4) TCID/50 MN 30-100 PRRSV. Following infection, animals were bled between days 0 to 135 pi. Viremia was detected up to day 30. Serum antibody response (by enzyme-linked immunosorbent assay [ELISA] and virus neutralization antibody) was detected from day 14 to 120 pi. Cell-mediated immune response represented by interferon gamma (IFN-gamma) was detected from day 14 to 120 pi. Persistence of PRRSV in tissues was confirmed by reverse transcriptase polymerase chain reaction (RT-PCR) between days 30 to 135. These results indicate that serum neutralizing antibodies and IFN-gamma play an important role in the clearance of PRRSV. Nevertheless none of the parameters measured (virus neutralizing antibodies), either alone or in combination, are solely responsible for the clearance of the virus from the host and the development of sterilizing immunity.
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PMID:Virological and immunological responses to porcine reproductive and respiratory syndrome virus in a large population of gilts. 1558 Dec 21


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